4.6 Article

Cutting Edge: Candida albicans Hyphae Formation Triggers Activation of the NlrP3 Inflammasome

Journal

JOURNAL OF IMMUNOLOGY
Volume 183, Issue 6, Pages 3578-3581

Publisher

AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0901323

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Funding

  1. National Institutes of Health [K08 AI065517, K08 AI067736]

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The proinflammatory cytokine IL-1 beta plays an important role in antifungal immunity;, however, the mechanisms by which fungal pathogens trigger IL-1 beta secretion are unclear. In this study we show that infection with Candida albicans is sensed by the Nlrp3 inflammasome, resulting in the subsequent release of IL-1 beta. The ability of C. albicans to switch from a unicellular yeast form into a filamentous form is essential for activation of the Nlrp3 inflammasome, as C. albicans mutants incapable of forming hyphae were defective in their ability to induce macrophage IL-1 beta secretion. Nlrp3-deficient mice also demonstrated increased susceptibility to infection with C. albicans, which is consistent with a key role for Nlrp3 in innate immune responses to the pathogen C. albicans. The Journal of Immunology, 2009, 183: 3578-3581.

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